Peripheral sympathetic neurodegeneration drives cardiac dysfunction in dominant optic atrophy, revealing a critical neuro-cardiac link. Optic atrophy factor-1 haploinsufficiency disrupts mitochondrial dynamics and neurotrophic signaling, causing targeted sympathetic denervation and arrhythmias. Restoring nerve growth factor transport and mitochondrial health in sympathetic neurons represents a promising therapeutic avenue for cardiac autonomic disorders. Future research must unravel mechanisms of neurocardiac crosstalk to develop precise interventions against neurogenic cardiac disease progression.
Ronfini et al. (Sun,) studied this question.